The factors which affect glomerular filtration rate will be examined utilizing micromeasurements of pressures, flows, permeabilities and filtration rates in the Munich-Wistar rat. Studies will further examine the specific mechanisms leading to the reduction in filtration following immune injury to the glomerulus. The effects of complement depletion and blockade of the renin-angiotensin system upon the previously observed reductions in glomerular permeability and plasma flow will be examined. Additional studies focus upon the specific mediators of the tubulo-glomerular feedback system for the control of glomerular filtration. We have demonstrated that variations in tubular reabsorption between late proximal and distal tubule produces reciprocal reductions in filtration rate in the same nephron unit. Angiotensin II (AII) has been proposed as a potential mediator of this response. Blockers of AII receptors and AII synthesis will both be utilized to determine if blockade of this intrarenal hormone modifies the previously demonstrated quantitative influence of changing tubular reabsorptive rates upon filtration rate. Chloride ion has been postulated as the critical reabsorbed material which triggers this tubulo-glomerular feedback response. We plan to further elucidate the relationship of water and chloride reabsorption between late proximal and distal tubules and characterize the influence of changing the rate of perfusion from the late proximal tubule. Related studies on the relation of peritubular capillary and interstitial hydrostatic and oncotic pressures to the rate of proximal tubular reabsorption will be further examined during partial renal venous occlusion (and compared to modest expansion with saline solutions). This model has been utilized to support the concept of peritubular control of proximal tubular reabsorption. All relevant pressures will be measured and applied to a mathematical model of peritubular capillary reabsorption.